Allergic contact dermatitis

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Allergic contact dermatitis is a common inflammatory condition that is characterized by erythema and pruritus at the site of exposure to an allergen. Common allergens include nickel, personal care products such as fragrances and cosmetics, topical medications, and plants. The underlying pathophysiology is a type IV, T-cell mediated delayed hypersensitivity reaction to the allergen. It is more common in women than men and impacts around 20% of the general population. Diagnosis is usually clinical, although patch testing is considered the gold standard and can be utilized if the causative allergen is unclear. Avoidance of allergen exposure is the mainstay of therapy. Topical corticosteroids and symptomatic therapy (e.g., with calamine lotion and emollients) are used to provide acute relief.

• 15–20% of adults have a contact allergy to ≥ 1 allergen. ^[2][3]
• ♀ > ♂ ^[3]

Allergic contact dermatitis is one of the most common dermatological diagnoses and its prevalence is increasing worldwide. ^[2]

Epidemiological data refers to the US, unless otherwise specified.

Common allergens ^[4][5]

• Metals: : nickel , cobalt, chromium ^[3]
• Personal care products: perfumes, soaps, cosmetics
• Plants: poison ivy, poison oak, poison sumac
• Occupational: gloves , solvents, detergents
• Preservatives: e.g., thimerosal
• Topical medications: hydrocortisone, topical antibiotics (e.g., neomycin), benzocaine ^[6]

Risk factors ^[2][7]

• Congenital risk factors: certain genetic polymorphisms
• Acquired risk factors: other forms of dermatitis (e.g., atopic dermatitis ), occupational exposures

Allergic contact dermatitis is an example of a type IV hypersensitivity reaction.

• First contact with allergen → sensitization
• Repeated contact with allergen → development of a rash after 12–48 hours

Compared to type I-III hypersensitivity reactions, which are antibody-mediated, type IV reactions are mediated by T cells.

• Characteristics of lesions ^[6]
  • Intensely pruritic erythematous papules
  • Vesicles with serous oozing in more severe cases
  • Distinct borders that correspond to the site and extent of exposure
• Distribution
  • Local (reflects areas and shapes of exposures); examples include:
    • Rash where jewelry is worn: suggests nickel allergy
    • Rash on face and eyelids: likely caused by cosmetics
    • Rash in axillae: likely caused by fragrances or deodorant
    • Pruritic papulovesicular rash with a linear pattern on extremities: likely caused by urushiol-producing plants like poison ivy in patients with a history of exposure (urushiol-induced contact dermatitis)
  • Ectopic (lesions at a distance from initial exposure): due to inadvertent transfer of allergen by self or others ^[7]

Contact dermatitis due to poison oak, poison ivy, or poison sumac is the most likely cause in a patient presenting with erythematous, pruritic, and burning skin lesions in a linear pattern that appear 24 hours after a camping trip.

Approach ^[6]

• Suspect allergic contact dermatitis in patients with pruritic lesions in well-demarcated areas of exposure.
• Review the patient's use of personal products as well as their home and work environment to determine the likely allergen. ^[7]
  • Cause is evident: Start management empirically.
  • Cause is unclear or lesions do not resolve with empiric management: Consider referral to an allergist or dermatologist for further evaluation.

Allergic contact dermatitis is primarily a clinical diagnosis. Diagnostic studies may be required in certain cases.

Patch test ^[8]

• Indications
  • Uncertain clinical diagnosis
  • Inadequate response to empiric management
  • Worsening of lesions on application of empirical topical therapy including corticosteroids ^[7]
  • Suspected contact dermatitis in children ^[7]
• Procedure
  • A series of patches fixed with common allergens are applied directly to the skin.
  • Results are commonly read at 48 hours. ^[7][8]
• Interpretation: A positive reaction consists of erythema, papules, and, sometimes, vesicles at the site of the patch(es). ^[9]

Before performing a patch test, avoid or decrease the dosage of systemic immunosuppressants (e.g., systemic corticosteroids). ^[7]

Additional studies ^[6]

Consider on a case-by-case basis, mostly to rule out differential diagnoses of contact dermatitis.

• Bacterial culture: if there is weeping, crusting, exudate
• KOH preparation: if there is erythema and scaling
• Punch biopsy: if the diagnosis remains unclear

• Irritant contact dermatitis (see “Irritant vs. allergic contact dermatitis”)
• Atopic dermatitis
• Seborrheic dermatitis
• Dyshidrotic eczema
• Psoriasis
• Scabies
• Tinea pedis
• Dermatitis herpetiformis
• Mycosis fungoides (cutaneous T-cell lymphoma)

The differential diagnoses listed here are not exhaustive.

Avoidance of exposure to allergens is the mainstay of management for allergic contact dermatitis. In addition, the following adjunctive measures should be initiated for acute relief. ^[6][7]

• Symptomatic therapy
  • Cool compresses
  • Calamine lotion, emollients, colloidal oatmeal baths
  • Wet dressings (e.g., for oozing, crusting lesions)
• Corticosteroids
  • Topical corticosteroids are preferred for localized dermatitis. ^[7]
    • Initial treatment: mid-potency topical steroid (e.g., triamcinolone ) ^[6]
    • No clinical improvement: Escalate to a high-potency topical steroid (e.g., clobetasol ). ^[6]
  • Consider systemic steroids (e.g., prednisone ; ) ^[6]
    • If > 20% of the body surface area is affected
    • Or if rapid relief is desired (e.g., involvement of the face and eyelids).
• Treatment of bacterial and fungal superinfections: See “Impetigo” and “Treatment of mucocutaneous candidiasis” as needed.

Use low-potency topical steroids (e.g., desonide) on areas of thinner skin (e.g., face, genitals, flexural surfaces). ^[6]

Avoid long-term use of topical steroids to prevent local skin atrophy and systemic side effects. ^[7]

Antihistamines, though commonly used, are generally not effective for treating pruritus associated with allergic contact dermatitis. ^[6]